Detrimental effects of post-treatment with fatty acids on brain injury in ischemic rats

Protective effect of docosahexaenoic acid against brain injury in ischemic rats

“…These experimental findings show some similarities with those clinical observations indicating lower proportions of PUFAs in stroke patients, and the reduction parallels stroke severity [21][22][23][24]. According to these relevant studies, the neuroactive effects of ω-3 PUFAs could be demonstrated in different administration routes, including oral gavage or intracerebroventricular, intravenous or intraperitoneal injection [26][27][28][29][30][32][33][34]. Surprisingly, the administration of DHA (100 nmol/kg ip) was ineffective in modulating postischemic alterations in this study.…”

“…Single injection of linolenic acid (167 nmol/kg icv or 100 nmol/kg iv) 30 min before stress prevents ischemia-induced neuronal loss [29]. However, acute posttreatment with DHA (500 nmol/kg ip) after ischemia remarkably exacerbated cerebral I/R injury [27]. In the present study, we found that intraperitoneal administration of DHA (500 nmol/kg) once 1 h or 3 days prior to ischemia attenuated postischemic brain injury.…”

“…During this period, elevation of fatty acids could be one of the consequent results of ischemic-insult-induced membrane disruption or one of the detrimental factors involved in postischemic progression after active release. Acute posttreatment with PUFAs, possibly further elevating free fatty acids, augments postischemic brain injury, indicating the possibility of the latter hypothesis [27]. This augmented effect could be partly mediated by enhancement of oxidative burden.…”

“…These observations have implications for the involvement of fatty acids in the initiation and/or progression of postischemic brain injury. Recently, we found that acute posttreatment with PUFAs after ischemia remarkably exacerbated cerebral I/R injury partly through augmented oxidative burden [27]. However, there is now considerable research describing the beneficial effects of PUFAs on the prevention of cerebral I/R injury in both human and animal studies.…”

Eicosapentaenoic Acid Prevents Memory Impairment After Ischemia by Inhibiting Inflammatory Response and Oxidative Damage

“…37 Thus, the tissue concentration may have been insufficient after just 1 week of EPA treatment, and this delayed distribution to the tissues may explain the ineffectiveness of short-term preischemic or postischemic n-3 EFA treatment. 38,39 These findings suggest that EPA may not be suitable for emergency care; however, because EPA has a long half-life, 37 intermittent administration after achievement of steady-state may be effective.…”